Most people still believe the only way to lose excess body fat is to follow a restricted calorie diet. This they believe will cause a negative calorie balance that will result in the utilisation of excess body fat as energy. However, central obesity is not caused by a positive energy balance, but is instead a metabolic dysfunction caused by high intakes of dietary fructose. The metabolic abnormalities associated with central obesity include insulin resistance, and this in turn causes leptin insensitivity in the hypothalamus. Under normal circumstances leptin signals the hypothalamus regarding the degree of fat present. As leptin resistance develops, the hypothalamus receives a weaker signal which is interpreted as resulting from low fat reserves and a starvation state. As a result the hypothalamus alters physiology to increase appetite, decrease physical activity and lower the thermic effects of food, in an effort to maintain current weight and prevent body fat loss.
Forcing the issue by undertaking physical activity and restricting calories by ‘dieting’ intensities the efforts by the hypothalamus to prevent weight loss, and as a result the resting metabolic rate (RMR) is lowered. Forced calorie restriction diets therefore are counter productive because they cause a homeostatic impasse that cannot be overcome by energy restriction. Further, it is known that the RMR of previously obese subjects is permanently depressed following forced calorie restriction because of long-term damage to metabolic regulation. For example, in one study1, researchers measured the RMR of previously obese subjects in comparison to normal weight individuals who had never been obese. The researchers made the RMR comparison at different levels of physical activity. The results showed that irrespective of the level of physical exertion, the formerly obese individuals had RMR that were around 15% lower than the lean controls.
The subjects in this study had been selected from local slimming clubs, which suggests they would have followed traditional forced calorie restriction diets in combination with increased physical activity. These results therefore support the contention that formerly obese subjects who have undertaken a forced calorie restrictive diet may have permanent damage to their RMR. This is despite the fact that obese individuals prior to ‘dieting’ have been shown to have RMR that are higher than lean counterparts. The authors noted that the obese individuals required less calories to sustain their normal body fat levels when compared to the lean controls, suggesting that resumption of normal eating patterns would have caused accelerated weight gain in these individuals. This explains the poor success rate of prescriptive forced calorie restriction diets common in slimming clubs.
Not surprisingly, the aerobic exercise performed in the study had little effect on RMR beyond the end of the exercise session undertaken. Therefore aerobic exercise is a poor choice of exercise when attempting to lose body fat because it has little impact on RMR. In contrast, resistance training leads to the hypertrophy of skeletal muscle, which is beneficial because muscle mass is the primary driver of RMR. In fact the reason that formerly obese individuals have low RMR is because during forced calorie restriction, skeletal muscle is catabolised through the gluconeogenic pathway, reducing the lean mass of the individual. A simple calculation shows that 45 minutes of light aerobic exercise increases energy expenditure by around 100 kcal. A similar figure can be achieved through addition of 20 to 25 grams per day of fibre to the diet, because fibre decreases the absorption efficiency of food by 3 to 4% through the decreased density of the bolus. So why bother with the hamster training?
RdB
